Typically, anti-viral agents are modelled to inhibit viral replication within an infected cell. Viral replication may be prevented by down-regulation or inhibition of a protein required in the viral replication pathway, or by interference with the translocation of proteins and viral nucleic acid within the cell. Effective anti-viral agents specifically target steps within the viral replication pathway thereby inhibiting or hindering viral replication within infected host cells while having a minimal cytotoxic effect on the host. Thus, many anti-viral agents are specific inhibitors to virus-specified enzymes and proteins, such as viral DNA and RNA polymerases, virus-specific thymidine kinase and cleavage enzymes for viral capsid protein. Nucleoside analogues, for example, have been developed which target particular enzymes in the viral replication pathway by mimicking a natural substrate of the enzyme.
Adverse toxicity effects exist with the administration of most anti-viral agents, particularly at the dosage levels required to attain effective antiviral chemotherapy, due to a lack of viral specificity. The adverse effects associated with the administration of some anti-viral agents are not as severe as those associated with other agents; nonetheless, such adverse effects do exist. Presently, there are very few anti-viral agents which are considered to be efficacious, i.e. agents having a high level of viral toxicity and a low level of cytotoxicity. accordingly, there is a need to develop anti-viral agents having an effective level of anti-viral activity while exhibiting minimal cytotoxicity, i.e. having a desirable therapeutic index.
It is a general object of the present invention to provide novel guanidino-substituted compounds having anti-viral activity, and compositions containing these compounds.
It is another object of the present invention to provide a method of treating a mammal infected with a herpesvirus.